FURTHER STUDIES ON THE RATE OF DISAPPEARANCE OF LABELLED THYROXINE FROM THE INTRAVASCULAR COMPARTMENT OF MAN, WITH REFERENCE TO THE ROLE OF THYROXINE BINDING PROTEINS

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Abstract
The disappearance of an intravenously injected tracer dose of 131I-labelled L-thyroxine [T4] from the circulation has been followed for 70 minutes. We have confirmed that the most significant separation between euthyroid subjects and patients with hyperthyroidism or myxoedema is given by the single exponential slope of the regression of blood radioactivity occurring between 20 and 50 minutes after T4 injection. This slope is referred to as the acute T4 half-time. When there is no alteration in total TBG [thyroxine-binding globulin] the acute T4 half-time is closely related to the plasma BEI [butanol extractable iodine] concentration. Increase in the latter due to Graves'' disease, toxic nodular goitre, or exo-genous administration of thyroxine or desiccated thyroid, results in a comparable acceleration in the acute T4 half-time compared to the value in euthyroid control subjects. Conversely patients with a low BEI due to primary or radioactive iodine induced myxoedema all have a singificantly slow acute T4 half-time compared to normal subjects. There was no specific abnormality in the handling of thyroxine by patients with Graves'' disease in contrast to the earlier findings of Lennon et al. (1961). Hypermetabolism per se does not affect the acute T4 half-time. The administration of pharmacological doses of triiodothyronine, unlike similar doses of thyroxine, failed to affect the acute T4 half-time. The acute T4 half-time is consistently related in an inverse manner to the concentration of unsaturated thyroxine-binding sites in association with TBG. These data show no such correlation between TBPA [thyroxine-binding prealbumin] binding and the acute T4 half-time. Synthetic oestrogen, by increasing the unsaturated thyroxine-binding capacity of TBG, produces a pro-found slowing of the acute T4 half-time.